The overall objective of this project is to investigate basic neuronal mechanisms underlying experimental amblyopia. Our working hypothesis is that neuronal inhibition in the visual cortex plays a major role in amblyopia. This is based upon our findings that the GABA antagonist bicuculline and naloxone are capable of restoring binocular input to visual cortical neurons in the cat. Recently, we showed bicuculline to be effective when administered microiontophoretically. Major activities for the coming year will be as follows: (1) to investigate the action of microiontophoretically applied agents upon visual cortical neurons in amblyopic cats. We will study effects upon both binocularity and visual acuity. The latter will be studied using a computer-driven optical system to quantitatively measure neuronal receptive field properties and to measure spatial grating sensitivities. In addition we will study agents in a behavioral paradigm measuring visual acuity. (2) to study amblyopia in an animal model which does not involve molecular deprivation. Using goggles, we have raised kittens in a visual environment in which each eye receives fully formed, focused input; however, one input is "scrambled" by a frequently rotated prism. This environment produces an amblyopic condition in the "scrambled" eye. We will be investigating the neurophysiology, neuropharmacology and neuroanatomy of this condition, comparing the results to those produced by monocular deprivation and strabismus. (3) to study GABA receptors in the visual system via autoradiography of labeled igands.